Fibrosis is a disease characterized by the excessive accumulation of a connective tissue component, and one which is a noticeable component in fibrosis is collagen.
Accumulation of collagen occurs in a variety of viscera, for example, brings about pulmonary fibrosis in lung and liver fibrosis in liver. Also in skin, for example, the accumulation of collagen brings about disorders such as cutis keloid formation.
In many cases, the net accumulation of collagen in fibrosis is the result of disproportion between factors which bring about decomposition and production of collagen.
Though various medications have been conducted to treat the disorder and sickness of fibrosis, they were mainly for symptomatic therapy for the disorder in general, and were not those which aim at dissolving pathogenesis, namely the disproportion between metabolism factors which regulate decomposition and production of collagen and the other connective tissue component. Therefore, in these therapies, there was no especially effective method in point of tissue repair. For example, though local corticosteroid was used to treat the initial inflammation stage of cutis keloid formation and success was made to a certain extent, such steroid treatment has little or no effect on the latter fibrosis stage such as in case of actual formation of keloid as a result of excessive production of collagen.
As described above, in the prior art, there could not have been discovered a safe and effective method which treats fibrosis disorder of human, inhibits more formation of fibrous tissue and reduces or completely removes the focus of fibrosis previously formed.
The object to be solved by the present invention is to provide an agent accelerating collagen decomposition which can induce the decomposition of a collagen matrix of excessively accumulated connective tissue in tissue and a therapeutic agent useful for treatment of fibrosis disorder.